Prostaglandin E1 (PGE1) suppresses water intake elicited by a number of dipsogenic agents. This suppression of water intake is maximal when the ingestion of water is initiated by increased blood and/or brain levels of angiotensin II (A II), a peptide hormone derived from renin. In addition, increased levels of A II stimulate the production and release of prostaglandins of the E series in a variety of organs. This suggests that rises in A II levels which initiate drinking might also stimulate the production of PGE in brain. This newly synthesized PGE could act in A II-sensitive neural sites or in interrelated neural areas to signal satiety and terminate a drinking bout. A II also acts centrally to increase systemic blood pressure and recent evidence suggests that central receptors for both the A II dipsogenic and pressor effects are located in the same neural area(s). The overall objective of the proposed research is to elucidate further the interactions between A II and PGE in the CNS regulation of water intake and blood pressure. One section of this proposal analyzes the role of endogenous PGE in the control of water intake initiated by A II through pharmacological blockade of prostaglandin synthesis. If a rise in brain levels of PGE does act as a satiety signal, prevention of PG synthesis should result in an increase of water intake under these conditions. Another section analyzes the role of endogenous and exogenous PGE in the central regulation of blood pressure and the interaction between these effects and the A II pressor response. The final section examines the sensitivity of neural sites reported to be involved in the production and/or mediation of the A II dipsogenic effect to PGE antidipsogenesis through the determination of threshold doses of PGE needed to suppress drinking when the PG is applied directly to those areas.